Osteoarthritis Flashcards
What is OA?
Symptoms?
- wearing out of hyaline articular cartilage of diarthrodial joints
- considered non-inflammatory, most common cause of chronic arthritis
- joint pain, inactivity stiffness, decreased ROM
Causes leading to OA
- age
- injury
- obesity
- chronic inflammation of joint
- Paget’s (abnormal stiff subchondral bone)
- Avascular necrosis (abnormal weak subchondral bone)
- in hip specifically - shallow acetabulum, femoral head tilt, femoral acetabular impingement
Where is OA common?
- large weight-bearing joints like hips/knees
- knee OA is most common
- can also be in the hands (DIPs, PIPs)
Effect of OA on knees
- Varus deformity of the knees
Diarthrodial Joints
- mobile, peripheral
- hyaline articular cartilage made of type 2 collagen and aggregated proteoglycans
- surrounded by fibrous capsule lined by synovium
Describe articular cartilage - main cell present?
- chondrocytes are the only cells present - no blood or nerve supply, nutrients come from the synovial fluid
- chondrocytes produce both type II collagen and PGs
- # of chondrocytes is fixed once you reach adulthood
- does not regenerate once it wears out
- radiolucent (black/grey) on x-ray - not calcified
What happens at a cellular level in OA?
- chondrocytes multiply in lacunae to try and synthesize more matrix
- however, this cannot keep up with the up-regulation of matrix metalloproteases
- less PG aggregates due to cleaving at hook region by aggrecanase
Describe the matrix of articular cartilage
- 90% water - hydrophilia of PGs allows for compliance, deformability, shock absorption
- type II collagen - arranged in branch arches, helps prevent breakdown of PGs, tensile strength, impact loading
- proteoglycans - (-) charged combinations of protein and sugar
Describe the structure of a proteoglycan
- bottle brush configuration
- central core protein with GAGs attached (- charged and thus attract water)
- hook region near amino terminal (aka hyaluronic acid binding region) which allows multiple PGs (aggrecans) to attach to HA
What are the two different GAG types?
- chondroitin sulfate - larger, located superiorly (carboxyl end), mostly galactosamine disaccharides
- some revision from C-6s (adult) to C-4s (fetal) in OA
- keratin sulfate - shorter, located proximally (amino end), enriched in glucosamine
*core protein has a unique a.a. sequence that determines where these GAGs attach
What is happening in the knee joint during compression/ relaxation?
- compression - water released by PGs into synovial space
- relaxation - water reimbibed into cartilage
What are the different neutral matrix metalloproteases? What makes them?
- collagenase 1 (MMP 1) - targets type II collagen
- stromelysin (MMP 3) - targets PGs
- collagenase 13 (MMP 13) - targets type II collagen
*all made by chondrocytes
What up regulates MMPs?
What inhibits them?
- IL-1 (made by chondrocytes, which have an IL-1 receptor), plasmin
- normally TIMPs block MMPs, but in OA MMPs overwhelm
What happens in OA with regard to:
- water content
- PG aggregates
- collagen
- metachromatic stain
- surface
- chondrocyte number
- MMP enzymes
- subchondral bone
- osteophytes
- Initially there is swelling due to water influx, then water loss and the joint becomes dry
- PGs and collagen decrease
- There is decreased uptake in metachromatic staining
- Bone surface becomes irregular and fibrillated
- Chondrocyte # increases due to mitoses in brood capsules
- MMP enzymes increase
- Subchondral bone comes sclerotic and there is presence of osteophytes
inflammatory mechanisms in OA
synovitis, IL-1, crystals
Primary vs Secondary OA
primary - localized, generalized such as in hands
secondary - chronic inflammatory arthritis (RA), identifiable mechanical/ congenital/ metabolic factors (i.e. hemochromatosis)
Names of enlargements at DIPs and PIPs
DIPs - Heberden’s nodes
PIPs - Bouchard’s nodes
Examples of inflammatory back pain
- common sx
- ankylosing spondylitis, sero (-) spondyloarthropathy
- under 40, prolonged morning stiffness, better with activity and worse with rest, nocturnal awakening, alternating buttock pain
Examples of infiltrative back pain
- malignancy (primary or metastatic from breast/lung/ prostate)
- infections (discitis, osteomyelitis, epidural abscess, TB)
What are back pain red flags?
(really only need blood work or imaging if these are present)
- pain at rest or at night
- history of trauma
- history of malignancy
- B symptoms (fever, weight loss, night sweats)
- incontinence
- saddle anesthesia
- substance use disorder
- steroids or immunocompromised
- first episode after the age of 50
- decreased passive range of motion
- midline tenderness
- new or progressive neuro issue (spasticity)
- loss of balance, abnormal gait
Cauda Equina Syndrome
- sx
- dx
- tx
- occurs when end of the spinal cord (L4-S4) is compressed (tumor, disc, infection, metastases)
- acute or chronic back pain, saddle anesthesia (S3-5), bladder and bowel dysfunction (S2-3), lower leg weakness/ sensory changes
- Dx: CT or MRI
- Tx: emergency! surgical decompression
Discogenic Back Pain
- often a normal asymptomatic part of aging, do NOT treat imaging findings if no pain or symptoms
- however, can be DDD or a herniation
Degenerative Disc Disease (DDD)
- micro fracture of collagen and loss of PGs leading to a desiccated disc
- see disc space narrowing on X-ray
- chronic onset
Disc Herniation
- imaging
- sx
- often acute due to lifting/ specific injury
- best seen on CT/MRI
- weakness, dermatomic pain, reflex loss, can be lateralized or central
Facet Arthropathy
- sx
- imaging
- facet joints (aka zygaphyseal joints) are synovial with hyaline surface, thus prone to OA
- most commonly due to aging
- unilateral neck/ lower back pain in non-dermatomic pattern
- pain worse with leaning back/ lumbar extension/ lateral flexion
- CT/MRI most useful, bone scan can demonstrate increased uptake suggesting active bone turnover and pain
Spondylolithesis
- sx
- one vertebra is sitting forward on the one below it
- non-union, lysis, fracture
- often developmental variation of neural arches (spondylolysis)
- worse pain with forward flexion
Spinal Stenosis
- sx for both spinal and vascular
- dx
- narrowing of the spinal canal
- can be congenital, osteophytes from facet hypertrophy, central disc herniation, mass effect from tumor or abscess, ligaments flavour hypertrophy
- if spinal claudication - worse with walking, spinal claudication worse with walking, better with sitting, better with bending forward, walking uphill is easier
- if vascular claudication - worse with walking, better with stop and stand, risk factors for PVD/ artherosclerosis, abnormal ABI, weak pedal pulses
- Dx: CT or MRI
Neural Foraminal Stenosis
- facet joints narrow due to osteophytes
- leaning to the affected side increases pain
SI Ligament Sprain
- sx
- causes
- buttock pain, difficulty sitting or standing
- acute injury, overuse, muscle weakness, imbalance
Scoliosis
- sx
- sideways curvature of the spine
- mild or asymptomatic, if severe can cause pain and respiratory issues
- often genetic and will develop overtime in chidlhood
In summary, which back pain syndromes are worse with flexion and which are worse with extension?
worse with flexion - spondylolitheis, discogenic pain
worse with extension - facet arthropathy, spinal stenosis
Role of PTs and OTs in OA?
PT - self management, therapeutic exercise, PA guidelines, manual therapy
OT - joint protection (splints, orthoses, footwear), energy conservation, ADLs
What is general non-surgical/pharmacological treatment for OA/ back pain?
EVIDENCE BASED: education, self-management, exercise (esp. quad strengthening), weight loss (dose-response relationship)
- avoid bed rest
- canes (NOT poles) are recommended for knee and hip OA (use opposite from affected side, wrist crease level when standing in shoes)
- neuromuscular training, aerobic exercise, flexibility
- potentially orthotics i.e. knee unloader brace/ braces/ laser/ TENS/ acupuncture, etc.
What role do adipocytes have in OA?
- release leptons and adiponectins that can lead to joint damage directly
Oral treatments for OA
Acetaminophen - can push to 3-4g/day if normal kidney and liver function
NSAIDs - helps with inflammation and pain
Opiates - i.e. tramadol, tramacet… controversial, can try Tylenol T3s or start with tramadol
Duloxetine (SNRI) - moderate evidence for knee OA
Alternatives - ginger, apple cider vinegar, CBD oil
Cons of NSAIDs (non-selective and selective)
non-selective - gastropathy especially if over 55
- use PPI for protection
- COX-2 selective (celecoxib) - no effect on upper GI mucosa
Both - affect renal function, increase BP, CV risks, lower GI upset (do NOT give if IBD)
- if on them chronically, need to monitor liver and creatinine/ CBC
Topical anti-inflammatories or analgesics for OA
- diclofenac (voltaren) - some efficacy, 1st line
- capsaicin - less evidence, more for neuropathic pain
Injections
- injectable corticosteroids - i.e. kenalog, Depomedrol
- no more than 3 injections in one joint EVER, no more than 2-3 per year
- inhibit IL-1 and MMPs, decrease inflammation
- viscosupplementation/HA - not recommended, unclear efficacy, still widely done
- platelet rich plasma (PRP) - centrifuged platelets, GFs, and cytokines re-injected
- does NOT regenerate cartilage, no current evidence
Glycosamine Sulfate (GLS-500) and Chondroitin Sulfate
- provide GAG substrate
- inhibit IL-1 and MMPs
- however, no proven role yet
DMOADs
- disease modifying anti-OA drugs
- some efficacy seen in strontium and tetracycline - inhibit MMPs
Possible future treatments in OA
- cartilage/ chondrocyte transplants
- growth peptide
- TIMPs (tissue inhibitors of metalloproteases)
- mesenchymal stem cells, bone marrow aspirate concentrate
What are some tools used to assess outcomes in OA?
- WOMAC and AIMS2
OA history taking
- always ask about arthritis or psoriasis
What is an acute onset of joint pain likely to be?
- infection (septic arthritis) i.e MRSA, will see r-sided endocarditis
- trauma
- gout or pseudogout
- renters disease
Gout
- acute onset, older age, diuretics, beer, rich food, past history
- can get in the knee, but big toe most common
- will likely see high serum uric acid, check fasting lipids as often metabolic
- arthrocentesis (joint aspiration) - look for infection/ crystals (yellow parallel, negatively bi-refringent)
Pseudogout
- often caused by calcium pyrophosphate dehydrate crystals (CCPD)
- will see chonedrocalcinosis on xray
- blue parallel, yellow perpendicular crystals
Indications for surgery in OA
- Nonoperative management has been maximized
- Pain interfering with QoL
- Reasonable expectations of joint replacement from the patient
- Pathology resulting in adult arthritis
Knee - medial OA, over 60, correctable deformity, stable knee
Surgical treatment for Hip OA
- total hip arthroplasty - very successful, replacements last 30+ years
Surgical treatment for knee OA
- arthroscopic debridement
- arthroscopic microfracture
- autologous cartilage implantation
- allograft osteochondral transplant
- high tibial osteotomy
- knee arthroplasty
- arthroscopic debridement - not common but maybe if unstable meniscus
- arthroscopic microfracture - creating small fractures to stimulate bone marrow cells for cartilage regeneration
- best for small symptomatic lesions under 2cm
- requires careful rehab, mod improvement, but inconsistent results
- autologous cartilage implantation - great results
- take several cylindrical plugs from non-weight bearing zone to deficient area
- allograft osteochondral transplant - harvested from cadaver (needs immediate transplant)
- high tibial osteotomy - consider if medial compartment is arthritic and nothing else
- offloads the medial compartment by realigning the tibia
- good for young active patients with moderate arthritis in the medial compartment
- knee arthroplasty - partial or total, replaces entire tibiofemroal joint and patella
- not as good as total hip replacement
- meant to treat pain, NOT to restore athleticism
Contraindications for surgery in OA
- panarthroses
- young
- obese
- labourer
- varus over 10
- ACL deficiency
- crystalline/inflammatory arthropathy
